1. Field of the Invention
The present invention relates to mice having a gene responsible for the spontaneous development of Type II diabetes.
2. Background Technology
Diabetes, in particular Type II diabetes (insulin-independent diabetes mellitus) has long been known as a lifestyle-related disease and is one of the diseases with a rapidly increasing number of patients worldwide. Although a drastic change in lifestyle is pointed out as a primary reason for such a rapid increase in the number of patients, a genetic factor is also significantly involved. The rapid increase in the number of patients presses the urgency for the development of an appropriate method for the prevention and treatment of diabetes, the elucidation of a causative gene and the clarification of the onset mechanism. For this purpose, an appropriate disease model animal is indispensably needed. In particular, a spontaneous disease model animal is useful in elucidating a causative gene and the like.
Examples of conventionally reported model animals which spontaneously develop Type II diabetes include KK-Ay mice (Nishimura M., Exp. Anim. 18, 147–157, 1969), NSY mice (Ueda H., et al., Diabetologia 38, 503–508, 1995), db/db mice (Hummel K. P., et al., Science 153, 1127–1128, 1966), ob/ob mice (Herberg L. & Kley H K, Horm. Metab. Res. 7, 410–5, 1975), and AKITA mice (Yoshioka M., et al., Diabetes 46, 887–894, 1997).
Of these animals, KK-Ay mice and NSY mice are models with obesity and db/db mice and ob/ob mice are models with obesity due to an abnormality in leptin receptors or in leptin production. On the other hand, AKITA mice are a model for diabetes caused by an abnormality in pancreatic β cells.
On the other hand, most of diabetes patients in Japan, of which more than 90% are Type II diabetes patients, are known to be nonobese Type II diabetes patients without obesity. Therefore, the development of model animals for Type II diabetes without obesity has been desired since conventional Type II diabetes model animals are not satisfactory to elucidate the cause of nonobese Type II diabetes and to establish a method for the treatment thereof.
As a nonobese Type II diabetes model animal, for example, a model mouse is so far reported in Japanese Patent Laid-Open Publication No. 2004-65181. This mouse exhibits abnormal insulin secretion.
The onset and symptoms of Type II diabetes are known to be closely associated with two factors, a decrease in insulin secretion and a decrease in insulin sensitivity (insulin resistance).